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PubMed2005

Curcumin inhibits platelet-derived growth factor-stimulated vascular smooth muscle cell function and injury-induced neointima formation.

OBJECTIVE: Vascular smooth muscle cell (VSMC) migration, proliferation, and collagen synthesis are key events involved in the pathogenesis of cardiovascular disease. Growth factors, such as platelet-derived growth factor (PDGF) and fibroblast growth factor, released during vascular injury plays a pivotal role in regulating these events. Curcumin (diferuloyl methane), a major component of the spice turmeric (Curcuma longa), has been shown recently to have beneficial effects in chronic conditions, such as inflammation, cancer, cystic fibrosis, and Alzheimer's disease. The objective of this study was to investigate the ability of curcumin to inhibit PDGF-stimulated migration, proliferation, and collagen synthesis in cultured VSMCs and neointima formation after carotid artery injury in rats. METHODS AND RESULTS: Curcumin (1 to 25 microM) produced a concentration-dependent inhibition of PDGF-elicited VSMC migration, proliferation, and collagen synthesis assessed by chemotaxis, [3H]thymidine incorporation, and [3H]-L-proline incorporation, respectively. Curcumin blocked PDGF-induced VSMC actin-cytoskeleton reorganization, attenuated PDGF signal transduction, and inhibited the binding of PDGF to its receptors. Carotid artery neointima formation was significantly attenuated by perivascular curcumin compared with vehicle controls 14 days after injury, characterized by reduced DNA synthesis, collagen synthesis, and PDGF receptor phosphorylation. CONCLUSIONS: These data suggest that curcumin is a potent inhibitor of key PDGF-stimulated VSMC functions and may play a critical role in regulating these events after vascular injury.

Actin Cytoskeleton↗

PubMed2005

Curcumin impregnation improves the mechanical properties and reduces the inflammatory response associated with poly(L-lactic acid) fiber.

We investigated poly(L-lactic acid) (PLLA) fibers and coils, simulating stents and the influence of impregnation with curcumin, a non-steroidal anti-inflammatory drug, intended to reduce the pro-inflammatory property of these implants. Fibers obtained by melt extrusion of 137 kDa PLLA resin containing 10% curcumin (C-PLLA) exhibited a stable curcumin release rate for periods up to 36 days. Curcumin increased the fiber tensile strength at break and decreased embrittlement vs. controls in 36 day 37 degrees C saline incubation. A mouse peritoneal phagocyte model was employed to test the anti-inflammatory properties of C-PLLA fibers in vitro. Myeloperoxidase and non-specific esterase activity assays were performed for adherent cells (polymorphonuclear leukocytes (PMN) and macrophages (MPhi), respectively). PMN and MPhi adhesion to C-PLLA fibers were significantly reduced compared to control PLLA fibers (2.6 +/- 0.91) x 10(5) vs. (5.6 +/- 0.67) x 10(5) PMN/cm2 and (3.9 +/- 0.23) x 10(3) vs. (9.1 +/- 0.7) x 10(3) MPhi/cm2 (P < 0.05), respectively. In addition, superoxide release in the phagocyte pool contacting C-PLLA fibers was 97% less than that for PLLA controls. A fresh human whole blood recirculation system was employed to analyze cell adhesion under flow conditions, employing scanning electron microscopy (SEM). Reduced adhesion of cells on C-PLLA fiber coils vs. controls was observed. These in vitro studies demonstrate that bulk curcumin impregnation can reduce the inflammatory response to bioresorbable PLLA fibers, whilst improving mechanical properties, thereby suggesting curcumin loading may benefit PLLA-based implants.

Animals↗

PubMed2006

Curcumin's biphasic hormetic response on proteasome activity and heat-shock protein synthesis in human keratinocytes.

Curcumin (diferuloylmethane), is a component of the yellow powder prepared from the roots of Curcuma longa (Zingiberaceae), also known as tumeric or turmeric. It is widely cultivated and used as a food ingredient in tropical areas of Asia and Central America. Treatment of mid-passage human epidermal keratinocytes with curcumin resulted in a biphasic hormetic dose-response with respect to proteasome activity. Curcumin treatment (up to 1 microM for 24 h) increased chymotrypsin-like activity by 46% compared to that in untreated keratinocytes. However, higher concentrations of curcumin were inhibitory, and at 10 microM the proteasome activity decreased to 46% of its initial value. Furthermore, the preincubation of human keratinocytes at 43 degrees C for 1 h, followed by 24-h treatment with 3 microM curcumin, led to an increase in heat-shock protein (hsp70 and hsp90) levels by 24% and 19%, respectively, and the effect was sustained at concentrations up to 10 microM. On the other hand, the level of the small hsp27 was unaffected by curcumin concentrations of 0.3-1 microM, while it decreased by 34% at 10 microM.

Adult↗

PubMed2005

Elucidation of anti-allergic activities of curcumin-related compounds with a special reference to their anti-oxidative activities.

The anti-allergic and anti-oxidative activities of curcumin-related compounds (glycosides, reductants and bis-demethoxy analogs) were investigated to elucidate the underlying active mechanisms and structural features of curcumin in exerting these activities. The anti-allergic activities were assessed by measurement of histamine release from rat basophilic leukemia cells, RBL-2H3. Curcumin and tetrahydrocurcumin (THC) caused a marked decrease in histamine release. Glycosides of curcumin, bis-demethoxycurcumin and THC also inhibited the release of histamine, though less potently than curcumin did. The anti-oxidative activities were assessed by measurement of cell-free or cellular radical scavenging. All compounds but diglycosides or bis-demethoxycurcumin analogs distinctly exerted anti-oxidative effects. The relationship between both of these activities revealed that all compounds with potent radical scavenging activities caused a definite decrease in histamine release, but some compounds with non-potent radical scavenging activities also inhibited the histamine release. These results suggest that the hydroxy groups of curcumin play a significant role in exerting both the anti-oxidative and anti-allergic activities, and that most of the compounds develop the anti-allergic activities through mechanisms related to anti-oxidative activities, but some through mechanisms unrelated to anti-oxidation activity.

Animals↗

PubMed2006

Turmeric and curcumin modulate the conjugation of 1-naphthol in Caco-2 cells.

Turmeric, the powdered dry rhizome of the Curcuma longa plant, and curcumin, the major anti-oxidant constituent of turmeric, have been shown to possess chemopreventive activity. To elucidate the possible interaction of turmeric and curcumin with conjugation reactions, which in many cases are involved in the activation of procarcinogens, we measured their effects in the conjugation of 1-naphthol in Caco-2 cells, a human colon carcinoma cell line, within a 24 h period. Turmeric exhibits inhibitory activity toward both sulfo- and glucuronosyl conjugations of 1-naphthol at approximately the same levels (IC(50)=0.24 and 0.29 mg/ml, respectively). Curcumin inhibits sulfo-conjugation at lower concentrations (IC(50)=9.7 microg/ml), but only showed weak inhibition toward glucuronosyl conjugation of 1-naphthol in Caco-2 cells. In addition, turmeric was found to strongly inhibit in vitro phenol sulfotransferase (SULT) activity and demonstrate moderate inhibitory properties against UDP-glucuronosyl transferase (UGT) activity in Caco-2 cells (IC(50)=0.17 mg/ml and 0.62 mg/ml, respectively). Curcumin also strongly inhibits in vitro phenol sulfotransferase activity with an IC(50) of 2.4 microg/ml. Moreover, and in contrast to the moderate inhibition of UGT activity by turmeric and curcumin, both induce the expression of the UGT1A1 and UGT1A6 genes, revealed by real-time PCR analysis. These findings are indicative of a possible interaction of both turmeric and curcumin with conjugation reactions in the human intestinal tract and colon. This in turn may affect the bioavailability of therapeutic drugs and toxicity levels of environmental chemicals, particularly procarcinogens.

Adenocarcinoma↗

PubMed2004

Effect of curcumin on radiation-impaired healing of excisional wounds in mice.

OBJECTIVE: To study the effect on wound contraction of pretreatment with various doses of curcumin (the most important active ingredient of the spice turmeric) in mice exposed to 6 Gy whole-body gamma radiation. METHOD: A full-thickness skin wound was produced on the dorsum of Swiss albino mice treated with and without 25, 50, 100, 150 or 200 mg/kg body weight of curcumin before exposure to 6 Gy gamma radiation. Progression of wound contraction was monitored using video images of the wound at various days post-irradiation until full healing occurred. Mean wound healing times were also calculated. RESULTS: Irradiation caused significant delay in wound contraction and healing times. However, treatment with curcumin resulted in a dose-dependent increase in contraction when compared with a control. Greatest contraction was observed for 100 mg/kg curcumin, with statistically significant results at days three (p < 0.009), six (p < 0.05) and nine (p < 0.05) post-irradiation for this dose. Complete healing was achieved by day 23 post-irradiation in the curcumin-treated irradiation group. CONCLUSION: Pretreatment with curcumin has a conductive effect on irradiated wounds. It could be a substantial therapeutic agent for ameliorating radiation-induced delay in wound repair in cases of combined injuries.

Analysis of Variance↗

PubMed2002

Curcumin's effects on sialic acid level and sialidase activity in Ehrlich ascites tumor bearing mice.

In this study, we determined curcumin's anticancer and chemopreventive effects in mice bearing Ehrlich ascites tumor by evaluation of cancer biomarkers, sialic acid level and sialidase activity. Both plasma sialic acid level and sialidase activity increased significantly in the mice group with Ehrlich ascites tumor. When the tumor groups fed with curcumin and fed with sesame oil were compared, sialic acid level and sialidase activity in ascites fluid significantly reduced in the group fed with curcumin in addition to the increases of plasma sialic acid level and sialidase activity. The tumor group fed with curcumin lived twice longer than the one fed with sesame oil. Curcumin as a phenolic compound decreased all these parameters in Ehrlich ascites tumors and lengthened survival by 88% in the mice with tumor. We concluded that curcumin has anticancer activity.

Animals↗

PubMed2006

Biological effects of curcumin and its role in cancer chemoprevention and therapy.

Curcumin, a natural component of the rhizome of curcuma longa has emerged as one of the most powerful chemopreventive and anticancer agents. Its biological effects range from antioxidant, anti-inflammatory to inhibition of angiogenesis and is also shown to possess specific antitumoral activity. The molecular mechanism of its varied cellular effects has been studied in some details and it has been shown to have multiple targets and interacting macromolecules within the cell. Curcumin has been shown to possess anti-angiogenic properties and the angioinhibitory effects of curcumin manifest due to down regulation of proangiogenic genes such as VEGF and angiopoitin and a decrease in migration and invasion of endothelial cells. One of the important factors implicated in chemoresistance and induced chemosensitivity is NFkB and curcumin has been shown to down regulate NFkB and inhibit IKB kinase thereby suppressing proliferation and inducing apoptosis. Cell lines that are resistant to certain apoptotic inducers and radiation become susceptible to apoptosis when treated in conjunction with curcumin. Besides this it can also act as a chemopreventive agent in cancers of colon, stomach and skin by suppressing colonic aberrant crypt foci formation and DNA adduct formation. This review focuses on the various aspects of curcumin as a potential drug for cancer treatment and its implications in a variety of biological and cellular processes vis-à-vis its mechanism of action.

Animals↗

PubMed1997

Some perspectives on dietary inhibition of carcinogenesis: studies with curcumin and tea.

Topical application of curcumin inhibits chemically induced carcinogenesis on mouse skin, and oral administration of curcumin inhibits chemically induced oral, forestomach, duodenal, and colon carcinogenesis. Curcumin and other inhibitors of cyclooxygenase and lipoxygenase are thought to inhibit carcinogenesis by preventing the formation of arachidonic acid metabolites. In contrast to our expectation of a tumorigenic effect of arachidonic acid, we found that treatment of 7,12-dimethylbenz[a]anthracene-initiated mouse skin with very high doses of arachidonic acid twice daily, 5 days a week for 26 weeks, failed to result in tumors. We considered the possibility that some of the cancer chemopreventive effects of curcumin may be related to an effect of this compound on cellular differentiation, and we investigated the effect of curcumin on differentiation in the human promyelocytic HL-60 leukemia cell model system. Although curcumin alone had little or no effect on cellular differentiation, when it was combined with all-trans retinoic acid or 1alpha,25-dihydroxyvitamin D3 a synergistic effect was observed. It is possible that many dietary chemicals in fruits, vegetables, and other edible plants can prevent cancer by synergizing with endogenously produced stimulators of differentiation such as all-trans retinoic acid, 1alpha,25-dihydroxyvitamin D3, and butyrate. More research is needed to test this hypothesis. Administration of green or black tea inhibits carcinogenesis in several animal models, and tumor growth is also inhibited. Several examples were presented of chemopreventive agents that inhibit carcinogenesis in one animal model but enhance carcinogenesis in a different animal model. Greater efforts should be made to understand mechanisms of cancer chemoprevention and to determine whether a potential chemopreventive agent is useful in many experimental settings or whether it is useful in only a limited number of experimental settings.

Animals↗

PubMed2004

[Effect of curcumin on extracellular matrix accumulation in the glomeruli in nephrotoxic sera nephritis rats].

OBJECTIVE: To observe whether curcumin could inhibit the accumulation of the collagen IV and fibronectin in the glomeruli in nephrotoxi sera nephritis rats. METHODS: Seventy-two healthy male Sprague-Dawley rats were divided into three groups, with 24 animals in each group. For normal control group, normal saline (0.5 ml/d) was injected through intra-caudal-vein for two days, and at the same time normal saline (0.5 ml/kg) was also daily administered intraperitoneally. For nephrotoxic sera nephritis group, nephrotoxic sera (0.5 ml/d) was injected through the tail vein for two days and dimethyl sulfoxide (0.5 ml/kg) was given intraperitoneally daily. For curcumin group, nephrotoxic sera was injected as above and meanwhile curcumin (50 mg.kg(-1).d(-1)) was administered intraperitoneally every day. Six rats in each group were killed on the 3rd, 7th, 14th and 28th day. Their renal tissue was fixed in 10% formalin for examining the expression of collagen IV and fibronectin. RESULTS: Minimal staining of collagen IV and fibronectin was detected in the basement membrane of normal control rats glomeruli. In the nephrotoxic sera nephritis rats and curcumin treated nephrotoxic sera nephritis rats, the accumulation of collagen IV and fibronectin was increased progressively, with significant difference in the accumulation of collagen IV (P<0.01) between these two groups at the same time points, while the significant difference in fibronectin accumulation (P<0.05) appeared only after the 7th days. CONCLUSION: Curcumin can reduce the accumulation of collagen IV and fibronectin in the glomeruli. Hence we postulated that curcumin might have beneficial effect for retarding glomerulosclerosis.

Animals↗

PubMed2006

Curcumin-attenuated trinitrobenzene sulphonic acid induces chronic colitis by inhibiting expression of cyclooxygenase-2.

AIM: To explore the possible mechanisms of curcumin in rat colitis induced by trinitrobenzene sulfonic (TNBS) acid. METHODS: Rats with TNBS acid-induced colitis were treated with curcumin (30 mg/kg or 60 mg/kg per day ip). Changes of body weight and histological scores as well as survival rate were evaluated. Leukocyte infiltration was detected by myeloperoxidase (MPO) activity assay. The expression of cyclooxygenase-2 (COX-2) was detected by RT-PCR and Western blot. Inflammation cytokines were determined by RT-PCR. Local concentration of prostaglandin E(2) (PGE(2)) in colon mucosa was determined by ELISA. RESULTS: Curcumin improved survival rate and histological image, decreased the macroscopic scores and MPO activity. Also curcumin reduced the expression of COX-2 and inflammation cytokines. In addition, treatment with curcumin increased the PGE(2) level. CONCLUSION: Curcumin has therapeutic effects on TNBS acid-induced colitis, the mechanisms seem to be related to COX-2 inhibition and PGE(2) improvement.

Animals↗

PubMed1998

[Study on the antimutagenicity of curcumin].

Curcumin is a coloring additive used in food, which has many biological functions. In order to provide basic information on its anticarcinogenicity, the antimutagenicity of curcumin was determined by Ames test and micronuclei test. The results indicated that curcumin (60-250 micrograms/plate) inhibited the revert mutant induced by 2, 7-diaminofluorene (2AF) with S-9 in TA98 and in TA100. The inhibitory rates are 29.5%-55.9% and 37.5%-59.1% respectively. Before the injection of cyclophosphamide (CP), mice were given with curcumin (60, 120, and 240 mg/kg) orally once a day for a week. The results revealed that curcumin reduced the micronuclei formation induced by CP. The inhibitory rates of curcumin are 43.7%, 56.9%, and 63.9% respectively, which are different from that of the positive control significantly.

Animals↗

PubMed2002

Curcumin inhibits cell cycle progression of immortalized human umbilical vein endothelial (ECV304) cells by up-regulating cyclin-dependent kinase inhibitor, p21WAF1/CIP1, p27KIP1 and p53.

To elucidate possible mechanisms of anti-angiogenic activity by curcumin, we performed cDNA microarray and found that curcumin modulated cell cycle related gene expression. For further confirmation, DNA contents and expression levels of cyclins, cyclin-dependent kinases (CDKs), and CDK inhibitors (CDKIs) were examined by FACS analysis and Western blotting, respectively. Curcumin was found to induce G0/G1 and/or G2/M phase cell cycle arrest, up-regulate CDKIs, p21WAF1/CIP1, p27KIP1, and p53, and slightly down-regulate cyclin B1 and cdc2 in ECV304 cells. However, expression level of other cyclins and CDKs were not changed by curcumin. We, therefore, conclude that the up-regulation of CDKIs by curcumin plays a critical role in the regulation of cell cycle distribution in these cells, which may have a major role in anti-angiogenic activity of curcumin.

Antineoplastic Agents↗

PubMed2002

Curcumin down-regulates AR gene expression and activation in prostate cancer cell lines.

Curcumin, traditionally used as a seasoning spice in Indian cuisine, has been reported to decrease the proliferation potential of prostate cancer cells, by a mechanism that is not fully understood. In the current study, we have evaluated the effects of curcumin in cell growth, activation of signal transduction, and transforming activities of both androgen-dependent and independent cell lines. Prostate cancer cell lines, LNCaP and PC-3, were treated with curcumin and its effects were further analyzed on signal transduction and expression of androgen receptor (AR) and AR-related cofactors using transient transfection assay and Western blotting. Our results show that curcumin down-regulates transactivation and expression of AR, activator protein-1 (AP-1), nuclear factor-kappaB (NF-kappaB), and CREB (cAMP response element-binding protein)-binding protein (CBP). Curcumin also inhibited the transforming activities of both cell lines as evidenced by the reduced colony forming ability in soft agar. The results obtained here demonstrate that curcumin has a potential therapeutic effect on prostate cancer cells through down-regulation of AR and AR-related cofactors (AP-1, NF-kappaB and CBP).

Antineoplastic Agents↗

PubMed2002

Curcumin activates the aryl hydrocarbon receptor yet significantly inhibits (-)-benzo(a)pyrene-7R-trans-7,8-dihydrodiol bioactivation in oral squamous cell carcinoma cells and oral mucosa.

The development of oral squamous cell carcinoma (SCC) shows a positive correlation with the carcinogen exposure that occurs during tobacco and alcohol use. The purpose of this study was to investigate whether the naturally occurring chemopreventive agent, curcumin, modulates expression and function of carcinogen- metabolizing enzymes in human keratinocytes isolated from oral SCC tumors. Dose-response studies demonstrated that curcumin concentrations of >or=25 micro M were cytotoxic for oral SCC cells. Curcumin increased both expression (reverse transcription-PCR analyses) and function (high-performance liquid chromatography determination of ethoxyresorufin metabolism) of cytochrome P-450 (CYP) 1A1 and/or CYP1B1. The aryl hydrocarbon receptor (AhR), which up-regulates a battery of genes associated with carcinogen metabolism, is activated by polycyclic aromatic hydrocarbons such as the tobacco-associated carcinogen benzo(a)pyrene. Electromobility shift assays demonstrated that similar to the established AhR ligand 2,3,7,8,-tetrachlorodibenzo-p-dioxin, curcumin inclusion resulted in AhR nuclear translocation and formation of the transcriptionally active AhR-aryl hydrocarbon receptor nuclear translocator complex. Cellular capacity to bioactivate the tobacco-associated carcinogen (-)-benzo(a)pyrene-7R-trans-7,8-dihydrodiodiol was determined by evaluating conversion of the carcinogenic metabolite diol epoxide to stable tetrols via high-performance liquid chromatography. Results of our metabolism studies showed that curcumin significantly inhibited CYP1A1-mediated benzo(a)pyrene diol bioactivation in both oral SCC cells and intact oral mucosa. Because CYP1A1 is one of the primary carcinogen-activating enzymes in oral mucosa, the use of curcumin as an oral cavity chemopreventive agent could have significant clinical impact via its ability to inhibit carcinogen bioactivation.

Adult↗

PubMed2002

[Effects of curcumin on proliferation and apoptosis in human hepatic cells].

OBJECTIVE: To investigate the effect of curcumin on the proliferation, cell cycle distribution and apoptosis of hepatocarcinoma cell line QGY. METHODS: The MTT method was used to assay the biologic activities of curcumin in different times and different doses. The cell cycle distribution was detected by flow cytometic analysis. The cell ultrastructure was observed by electronic microscopy. RESULTS: Curcumin could inhibit effectively QGY in a dose- and time- dependent manner. IC(50) of curcumin to QGY was 49.50 micromol/L in 72 hours. The cell growth was arrested at S stage. Curcumin could lead to the degeneration, necrosis, and apoptosis. CONCLUSIONS: Curcumin can interrupt the cell cycle and has a role in cytotoxicity, antiproliferation and inducing apoptosis of QGY.

Antineoplastic Agents↗

PubMed2000

[Regulation effect of curcumin on blood lipids and antioxidation in hyperlipidemia rats].

The regulation effects of curcumin on lowering blood lipids and antioxidation were studied in the hyperlipoidemia model Wistar rats fed with high fat diet for 4 weeks. The hyperlipoidemia model rats were then separated into four groups: normal diet group, normal diet + curcumin (5 g/kg) group, high-fat diet group and high-fat diet + curcumin group. The rats were fed with experimental diets for another 4 weeks respectively. The results indicated that curcumin decreased the serum levels of cholesterol and triglyceride and increased the serum level of apolipoprotein A. Curcumin decreased TBA value and improved total antioxidation capability. The activities of SOD and GSH-PX in liver were enhanced. After taking normal diet for four weeks, the blood fat and cholesterol levels of the hyperlipoidemia rats recovered. But in the normal diet + curcumin group, the same results could be found in two weeks.

Animals↗

PubMedDate not supplied

Turmeric (Curcuma longa) and curcumin inhibit the growth of Helicobacter pylori, a group 1 carcinogen.

BACKGROUND: Curcumin, a polyphenolic chemical constituent derived from turmeric (Curcuma longa), has been shown to prevent gastric and colon cancers in rodents. Many mechanisms have been proposed for the chemopreventative effects, although the effect of curcumin on the growth of Helicobacter pylori has not been reported. H. pylori is a Group 1 carcinogen and is associated with the development of gastric and colon cancer. MATERIALS AND METHODS: A methanol extract of the dried powdered turmeric rhizome and curcumin were tested against 19 strains of H. pylori, including 5 cagA+ strains. RESULTS: Both the methanol extract and curcumin inhibited the growth of all strains of H. pylori in vitro with a minimum inhibitory concentration range of 6.25-50 micrograms/ml. CONCLUSION: These data demonstrate that curcumin inhibits the growth of H. pylori cagA+ strains in vitro, and this may be one of the mechanisms by which curcumin exerts its chemopreventative effects.

Curcuma↗